At the time of infection of an E. coli cell with a T4 bacteriophage, that cell is presented with two sets of genetic instructions dictating two completely different pathways of metabolic activity. Under laboratory conditions, such T4-infected cells respond invariably to the dictations of the viral genome. We are studying this gentetic takeover of the host cell's metabolic machinery, which is the basis for the pathogenicity of viruses. We have constructed multiple mutant strains of phage T4 which fail to induce the three known T4-induced modifications of the functional host nucleoid, namely, DNA degradation, nuclear disruption, and unfolding of the folded genomes. These strains should provide a starting point for the identification of new mutations in genes involved in shutoff of host metabolism. Our current research is focused on the T4 genes coding for proteins that become associated with the host ribosomes after T4 infection. By comparative biochemical studies of ribosomes from cells infected with mutants carrying mutations in these genes and with wild-type phage, we hope to determine the roles of these viral genes.